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Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
Published on: October 25, 2013
Correlation between Reduced Daptomycin Susceptibility and Vancomycin Resistance in Vancomycin-Intermediate
Longzhu Cui1, Eiji Tominaga, Hui-Min Neoh
1Department of Bacteriology, Faculty of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan 113-8421. longzhu@med.juntendo.ac.jp
Abstract:
We present here findings of a strong positive correlation between reduced daptomycin susceptibility and vancomycin resistance in vancomycin-intermediate Staphylococcus aureus (VISA). This correlation is related to cell wall thickening, suggesting that, similar to the case with vancomycin resistance in VISA, the physical barrier of a thickened cell wall may contribute to daptomycin resistance in S. aureus.
Insights
Reduced daptomycin susceptibility strongly correlates with vancomycin resistance in vancomycin-intermediate Staphylococcus aureus (VISA). A thickened cell wall likely contributes to this daptomycin resistance in S. aureus.
Area of Science:
- Microbiology
- Infectious Diseases
- Pharmacology
Background:
- Staphylococcus aureus is a common cause of infections.
- Vancomycin resistance in S. aureus is a growing concern.
- Vancomycin-intermediate S. aureus (VISA) strains exhibit reduced susceptibility to vancomycin.
Purpose of the Study:
- To investigate the correlation between daptomycin susceptibility and vancomycin resistance in VISA.
- To explore the underlying mechanisms contributing to daptomycin resistance in VISA.
Main Methods:
- Analysis of daptomycin susceptibility testing in VISA isolates.
- Assessment of cell wall thickness in relation to antibiotic resistance.
Main Results:
- A strong positive correlation was observed between reduced daptomycin susceptibility and vancomycin resistance in VISA.
- Cell wall thickening was identified as a key factor associated with this correlation.
Conclusions:
- Thickened cell walls in VISA may act as a physical barrier, contributing to daptomycin resistance.
- Understanding this mechanism is crucial for developing effective treatment strategies against resistant S. aureus infections.
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